Impairment of hepatic growth hormone and glucocorticoid receptor signaling causes steatosis and hepatocellular carcinoma in mice

Growth hormone (GH)‐activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)‐responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the developmen...

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Published inHepatology (Baltimore, Md.) Vol. 54; no. 4; pp. 1398 - 1409
Main Authors Mueller, Kristina M., Kornfeld, Jan‐Wilhelm, Friedbichler, Katrin, Blaas, Leander, Egger, Gerda, Esterbauer, Harald, Hasselblatt, Peter, Schlederer, Michaela, Haindl, Susanne, Wagner, Kay‐Uwe, Engblom, David, Haemmerle, Guenter, Kratky, Dagmar, Sexl, Veronika, Kenner, Lukas, Kozlov, Andrey V., Terracciano, Luigi, Zechner, Rudolf, Schuetz, Guenther, Casanova, Emilio, Pospisilik, J. Andrew, Heim, Markus H., Moriggl, Richard
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.10.2011
Wiley
Wiley Subscription Services, Inc
Subjects
Analysis of Variance
Animals
Biological and medical sciences
Blotting, Western
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Disease Models, Animal
Fatty Liver - metabolism
Fatty Liver - pathology
Gastroenterology. Liver. Pancreas. Abdomen
Growth Hormone - metabolism
Hepatology
Hyperglycemia
Immunohistochemistry
Kinases
Lipids
Lipodystrophy - metabolism
Lipodystrophy - pathology
Liver Biology/Pathobiology
Liver cancer
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
MEDICIN
Medicin och hälsovetenskap
MEDICINE
Metabolism
Mice
Mice, Knockout
Random Allocation
Receptors, Glucocorticoid - genetics
Receptors, Glucocorticoid - metabolism
Reference Values
Risk Assessment
Rodents
Signal Transduction
STAT5 Transcription Factor - metabolism
Tissue Culture Techniques
Tumor necrosis factor-TNF
Tumors
Liver
Rodentia
Hepatic disease
Hepatocellular carcinoma
Malignant tumor
Steatosis
Somatotropin
Vertebrata
Mammalia
Mouse
Animal
Gastroenterology
Glucocorticoid receptor
Digestive diseases
Cancer
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Abstract Growth hormone (GH)‐activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)‐responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver‐specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double‐mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up‐regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP‐1) and peroxisome proliferator activated receptor gamma (PPAR‐γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5‐dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR‐deficient livers harbored dysplastic nodules and ∼60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF‐α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c‐Jun N‐terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis. (HEPATOLOGY 2011;54:1398–1409)
AbstractList Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR- gamma ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and 60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF- alpha ) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis. (HEPATOLOGY 2011; 54:1398-1409)
Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and ∼60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent.
UNLABELLEDGrowth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and ∼ 60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. CONCLUSIONHepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis.
Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and ˜60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis. (Hepatology 2011;54:1398–1409)
Growth hormone (GH)‐activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)‐responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver‐specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double‐mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up‐regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP‐1) and peroxisome proliferator activated receptor gamma (PPAR‐γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5‐dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR‐deficient livers harbored dysplastic nodules and ∼60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF‐α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c‐Jun N‐terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis. (HEPATOLOGY 2011;54:1398–1409)
Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-gamma) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and similar to 60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-alpha) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. Conclusion: Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis.
Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR) are important signal integrators in the liver during metabolic and physiologic stress. Their deregulation has been implicated in the development of metabolic liver diseases, such as steatosis and progression to fibrosis. Using liver-specific STAT5 and GR knockout mice, we addressed their role in metabolism and liver cancer onset. STAT5 single and STAT5/GR double mutants developed steatosis, but only double-mutant mice progressed to liver cancer. Mechanistically, STAT5 deficiency led to the up-regulation of prolipogenic sterol regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator activated receptor gamma (PPAR-γ) signaling. Combined loss of STAT5/GR resulted in GH resistance and hypercortisolism. The combination of both induced expression of adipose tissue lipases, adipose tissue lipid mobilization, and lipid flux to the liver, thereby aggravating STAT5-dependent steatosis. The metabolic dysfunctions in STAT5/GR compound knockout animals led to the development of hepatic dysplasia at 9 months of age. At 12 months, 35% of STAT5/GR-deficient livers harbored dysplastic nodules and ∼ 60% hepatocellular carcinomas (HCCs). HCC development was associated with GH and insulin resistance, enhanced tumor necrosis factor alpha (TNF-α) expression, high reactive oxygen species levels, and augmented liver and DNA damage parameters. Moreover, activation of the c-Jun N-terminal kinase 1 (JNK1) and STAT3 was prominent. Hepatic STAT5/GR signaling is crucial for the maintenance of systemic lipid homeostasis. Impairment of both signaling cascades causes severe metabolic liver disease and promotes spontaneous hepatic tumorigenesis.
Author Haindl, Susanne
Engblom, David
Hasselblatt, Peter
Moriggl, Richard
Esterbauer, Harald
Mueller, Kristina M.
Friedbichler, Katrin
Kratky, Dagmar
Pospisilik, J. Andrew
Kozlov, Andrey V.
Sexl, Veronika
Wagner, Kay‐Uwe
Kornfeld, Jan‐Wilhelm
Casanova, Emilio
Egger, Gerda
Terracciano, Luigi
Heim, Markus H.
Schlederer, Michaela
Schuetz, Guenther
Kenner, Lukas
Zechner, Rudolf
Blaas, Leander
Haemmerle, Guenter
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ContentType Journal Article
Copyright Copyright © 2011 American Association for the Study of Liver Diseases
2015 INIST-CNRS
Copyright © 2011 American Association for the Study of Liver Diseases.
Copyright © 2011 American Association for the Study of Liver Diseases 2011
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IsDoiOpenAccess true
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Issue 4
Keywords Liver
Rodentia
Hepatic disease
Hepatocellular carcinoma
Malignant tumor
Steatosis
Somatotropin
Vertebrata
Mammalia
Mouse
Animal
Gastroenterology
Glucocorticoid receptor
Digestive diseases
Cancer
Language English
License CC BY 4.0
Copyright © 2011 American Association for the Study of Liver Diseases.
Re-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c6969-cebbb69cc7624864439bf416a2336291c9471c7c96279a2fa959385bb92d23ec3
Notes These authors contributed equally to this work.
This work was supported by grant SFB F28 from the Austrian Science Funds (FWF; to R.M., J.W.K., K.M.M., V.S., and K.F.) and grant SFB F30 (FWF; to G.H., D.K., and R.Z.). G.E. was supported by an Elise Richter fellowship (FWF; V102‐B12). L.B. and E.C. were supported by grant GEN‐AU Austromouse. H.E. and J.A.P. were supported by grants of the Vienna Science and Technology Fund (WWTF project LS07‐058) and JDRF.
Re‐use of this article is permitted in accordance with the Terms and Conditions set out at
Potential conflict of interest: Nothing to report.
http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms
fax: (43)‐14277‐9641
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content type line 23
Additional Supporting Information may be found in the online version of this article.
View this article online at wileyonlinelibrary.com.
This work was supported by grant SFB F28 from the Austrian Science Funds (FWF; to R.M., J.W.K., K.M.M., V.S., and K.F.) and grant SFB F30 (FWF; to G.H., D.K., and R.Z.). G.E. was supported by an Elise Richter fellowship (FWF; V102-B12). L.B. and E.C. were supported by grant GEN-AU Austromouse. H.E. and J.A.P. were supported by grants of the Vienna Science and Technology Fund (WWTF project LS07-058) and JDRF.
Address reprint requests to: Richard Moriggl, Ph.D., Ludwig-Boltzmann-Institute for Cancer Research, Waehringerstrasse 13a, A-1090 Vienna, Austria. E-mail: richard.moriggl@lbicr.lbg.ac.at; fax: (43)-14277-9641.
OpenAccessLink https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fhep.24509
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PublicationTitle Hepatology (Baltimore, Md.)
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Snippet Growth hormone (GH)‐activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)‐responsive glucocorticoid receptor (GR)...
Growth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid receptor (GR)...
UNLABELLEDGrowth hormone (GH)-activated signal transducer and activator of transcription 5 (STAT5) and the glucocorticoid (GC)-responsive glucocorticoid...
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SubjectTerms Analysis of Variance
Animals
Biological and medical sciences
Blotting, Western
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Disease Models, Animal
Fatty Liver - metabolism
Fatty Liver - pathology
Gastroenterology. Liver. Pancreas. Abdomen
Growth Hormone - metabolism
Hepatology
Hyperglycemia
Immunohistochemistry
Kinases
Lipids
Lipodystrophy - metabolism
Lipodystrophy - pathology
Liver Biology/Pathobiology
Liver cancer
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
MEDICIN
Medicin och hälsovetenskap
MEDICINE
Metabolism
Mice
Mice, Knockout
Random Allocation
Receptors, Glucocorticoid - genetics
Receptors, Glucocorticoid - metabolism
Reference Values
Risk Assessment
Rodents
Signal Transduction
STAT5 Transcription Factor - metabolism
Tissue Culture Techniques
Tumor necrosis factor-TNF
Tumors
Title Impairment of hepatic growth hormone and glucocorticoid receptor signaling causes steatosis and hepatocellular carcinoma in mice
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fhep.24509
https://www.ncbi.nlm.nih.gov/pubmed/21725989
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https://search.proquest.com/docview/1776668598
https://search.proquest.com/docview/895853696
https://pubmed.ncbi.nlm.nih.gov/PMC3232450
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-71643
http://kipublications.ki.se/Default.aspx?queryparsed=id:123340955
Volume 54
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